The lung's metabolic and cellular responses to injury are poorly understood but we will use oxygen toxicity primarily to produce lung injury in animals and follow the metabolic changes while the exposure (injury) continues and during the recovery in air. The metabolic changes of interest to us are a series of enzyme activities including glucose-6-phosphate dehydrogenase, glutathione reductase, glutathione peroxidase, superoxide dismutase plus glutathione content and lipid synthesis (especially dipalmitoyl phosphatidylcholine). A phenomenon referred to as "tolerance" which develops following a sub-lethal injury to the lung is of particular interest to us. The capacity to tolerate increased exposure to injurious agents suggests to us that the lung has undergone cellular and metabolic changes which protect it from further injury. We hope to determine the nature of these changes. We are particularly interested in conditions which may promote the injury (such as poor perfusion or other types of injury) or alter the recovery in air. We also plan to determine some aspects of the pathways for synthesis of dipalmitoyl phosphatidylcholine and the significance of substrate delivery through the capillary where enzymes might alter the substrate and change its utilization.